peoniflorin and Myocardial-Infarction

To study the myocardial benefit effect and mechanism of paeoniflorin on myocardial ischemia reperfusion injury (MIRI) in rats.. Hundred SD rats were randomly divided into 5 groups: sham group, model group, Paeoniflorin (15 mg/kg) group, Paeoniflorin (30 mg/kg) group, and Paeoniflorin (60 mg/kg) group. Myocardial ischemia reperfusion model was established in each group except the sham group. The myocardial infarction and morphological changes were measured by the TTC staining and HE staining respectively. Myocardial caspase-3 was detected by immunohistochemistry. In addition, the protein levels of Bcl-2 and Bax and the expression ratio of p-erk, p-jnk, and p-p38 were detected by Western blot. Myocardial superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were measured by the assay kit.. Paeoniflorin (30 mg/kg) and Paeoniflorin (60 mg/kg) can obviously alleviate myocardial infarction caused by MIRI (p < 0.05). HE staining showed that the myocardial morphology in the treatment group was obviously better than that in the model group. WB and immunohistochemistry showed that Paeoniflorin (30 mg/kg) and Paeoniflorin (60 mg/kg) can significantly increase the reduced protein level of bcl-2 (p < 0.05) and reduce the increased protein level of caspase3, bax -p-erk, p-jnk, and p-p38 caused by MIRI (p < 0.05). The activity of SOD was increased and the level of MDA was decreased after Paeoniflorin treatment.. Paeoniflorin preconditioning has a protective effect on MIRI in rats. Its mechanism is related to reducing oxidative stress and apoptosis by inhibiting the expression of apoptosis-related signaling pathway.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Apoptosis; Cardiotonic Agents; Caspase 3; Glucosides; Male; MAP Kinase Signaling System; Medicine, Chinese Traditional; Monoterpenes; Myocardial Infarction; Myocardial Reperfusion Injury; Myocytes, Cardiac; Oxidative Stress; Random Allocation; Rats; Rats, Sprague-Dawley

Paeoniflorin (PF) is the active component of. In this study, AMI model was established by ligating the anterior descending coronary artery in Wistar rats. After 4 weeks gavage of PF, the apparent signs and the left ventricle weight index of Wistar rats were observed. The left ventricular ejection fraction (LVEF) was evaluated by Doppler ultrasonography. Changes in cardiac morphology were observed by pathologic examination, and apoptosis was observed by the terminal deoxynucleotidyl transferase dUTP nick end labeling assay. In addition, enzyme-linked immunosorbent assay was used to detect the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) interleukin-10 (IL-10) and brain natriuretic peptide (BNP). Immunohistochemistry and Western blot method were applied to detect Caspase-3 and Caspase-9.. Compared with the model control, the survival conditions of rats in all treatment groups were generally improved after PF treatment. LVEF was significantly increased, and both left ventricular end-diastolic inner diameter and left ventricular end-systolic inner diameter were significantly reduced. Moreover, pathologic examination showed that the myocardium degeneration of the rats treated with PF was decreased, including neater arrangement, more complete myofilament, more uniform gap and less interstitial collagen fibers. Furthermore, the mitochondrial structure of cardiomyocytes was significantly improved. The ultrastructure was clear, and the arrangement of myofilament was more regular. Also, the expression of Caspase-3 and Caspase-9 was inhibited, and apoptosis was obviously reduced in the PF treatment groups. BNP, TNF-α and IL-6 were also decreased and IL-10 was increased in the treated rats.. PF could significantly improve the LVEF of rats. It decreased adverse left ventricular remodeling after myocardial infarction in rat models. The potential mechanism could be that PF decreased and inhibited BNP, TNF-α and IL-6, increased IL-10 and further inhibited the expression of Caspase-3 and Caspase-9, thus promoting ventricular remodeling.

Topics: Acute Disease; Animals; Apoptosis; Disease Models, Animal; Glucosides; Heart Function Tests; Male; Monoterpenes; Myocardial Infarction; Myocardium; Rats; Rats, Wistar; Ventricular Function, Left; Ventricular Remodeling

Paeoniflorin (PF) is the main active component of the commonly used Traditional Chinese Medicine peony, Paeonia Suffruticosa. PF has diverse biological functions and exhibits anti‑oxidative, anti‑inflammatory and anti‑apoptotic activity. Inducible nitric oxide synthase (iNOS) is a catalyzing enzyme that is involved in the synthesis of nitric oxide (NO). NO has an important regulatory role in the cardiovascular, immune and nervous systems. PF has previously been demonstrated to inhibit the gene expression of iNOS. The present study aimed to identify a potentially novel cytoprotective function of PF, and to elucidate its effects against myocardial ischemic damage in a rat model of acute myocardial infarction (AMI). PF was able to significantly decrease the myocardial infarct size as well as the activities of creatine kinase (CK), the MB isoenzyme of CK, lactate dehydrogenase and cardiac troponin T. In addition, in the PF‑treated groups, the expression levels of tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and nuclear factor‑κB were markedly inhibited. Furthermore, treatment with PF inhibited the activities and protein expression levels of iNOS. Decreased caspase‑3 and caspase‑9 activities were also observed in the AMI rat model treated with various doses of PF. The results of the present study indicated that the cardioprotective effects of PF may be associated with the inhibition of inflammation and iNOS signaling pathways.

Topics: Acute Disease; Animals; Anti-Inflammatory Agents; Caspase 3; Caspase 9; Creatine Kinase; Creatine Kinase, MB Form; Cytokines; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Glucosides; Inflammation; L-Lactate Dehydrogenase; Medicine, Chinese Traditional; Monoterpenes; Myocardial Infarction; NF-kappa B; Nitric Oxide Synthase Type II; Paeonia; Rats; Rats, Sprague-Dawley; Signal Transduction; Troponin T

We aimed to detect optimal ratio of cardioprotection-dependent absorbed bioactive compounds (ABCs) as quality control of guan-xin-er-hao (GXEH) formula extracted by various processings.. Ferulic acid (F), tanshinol (T), hydroxysafflor yellow A (A), protocatechualdehyde (P) and paeoniflorin (E) in GXEH formula and FTA in blood from rat with acute myocardial infarction (AMI) were first identified by HPLC-MS/MS, and FTAPE in GXEH formulae with various herbs, extraction times and extraction water volumes were then quantitated only by HPLC.. FTAPE in various GXEH were determined. FTA were selected as GXEH's ABCs. Ratios of FTA were determined, suggesting the high (1:6.1:15.6), medium (1:1.7:15.2) and low (1:0.2:15.3) ratios. Three FTA ratios and their parent formulae ratio-dependently reduced infarct size, myocardial apoptosis and caspase-3 activity.. There is the optimal ratio of F:T:A among various formulae, contributing to the best cardioprotection. This FTA ratio was developed as quality control of GXEH formula.

Topics: Animals; Apoptosis; Benzaldehydes; Benzoates; Bridged-Ring Compounds; Cardiotonic Agents; Caspase 3; Catechols; Chalcone; Chemistry, Pharmaceutical; Coumaric Acids; Drugs, Chinese Herbal; Ethnopharmacology; Glucosides; Male; Monoterpenes; Myocardial Infarction; Phytotherapy; Quality Control; Quinones; Rats; Rats, Sprague-Dawley

We have used microarray technology to detect the effect of Guanxin No.2 decoction on gene expression in different areas of the myocardial infarcted heart of rats.. Male Sprague-Dawley rats (180-200 g) were randomly divided into three groups: sham-operated; coronary artery ligation; and coronary artery ligation plus administration of Guanxin No.2 decoction (10.0 g raw materials/kg per day by gavage). The experiment was carried out on day seven after ligation.. We found that the gene expression using microarray technology showed many differences in the border infarcted left ventricular area compared with the remote noninfarcted left ventricular area after administration of Guanxin No.2 decoction.. Guanxin No.2 decoction has a long history in treating ischaemic cardiomyopathy in China, but the molecular mechanism has been unclear. In this study we found that some important genes may have contributed to the cardioprotective effect of Guanxin No.2 decoction.

Topics: Animals; Benzaldehydes; Benzoates; Benzofurans; Bridged-Ring Compounds; Cardiotonic Agents; Carthamus tinctorius; Catechols; Chalcone; Coumaric Acids; Dalbergia; Drugs, Chinese Herbal; Gene Expression; Gene Expression Profiling; Glucosides; Heart Ventricles; Hydroxybenzoates; Lactates; Ligusticum; Male; Monoterpenes; Myocardial Infarction; Oligonucleotide Array Sequence Analysis; Paeonia; Plant Extracts; Quinones; Rats; Rats, Sprague-Dawley; Reverse Transcriptase Polymerase Chain Reaction; Salvia miltiorrhiza